The brains of Alzheimer’s disease patients have an abnormal build up of amyloid-β proteins and tau tangles, which, according to many researchers, drives the ultimately fatal cognitive disease. This theory is being amended to a newer one, which posits that microbes may trigger Alzheimer’s pathology. Two new studies, using different approaches, further bolster this pathogen theory. Analyzing the transcriptomes of post-mortem brain samples from patients with Alzheimer’s disease, one group of researchers finds that two strains of human herpes virus (Roseoloviruses HHV-6 and HHV-7) are significantly more abundant than in the brains of people of the same age without Alzheimer’s disease. Gene networks in the brains of Alzheimer’s patients with these strains are also rewired such that disease-related genes are differentially expressed compared to controls.
In the other study, another team of investigators observed in mouse models and in a three-dimensional human neuronal cell culture that a Herpesviridae infection could seed amyloid-β plaques.
In the other study, another team of investigators observed in mouse models and in a three-dimensional human neuronal cell culture that a Herpesviridae infection could seed amyloid-β plaques.
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